IL-6 and Stat3 Are Required for Survival of Intestinal Epithelial Cells and Development of Colitis-Associated Cancer
Sergei I. Grivennikov,Eliad Karin,Janoš Terzić,Janoš Terzić,Daniel Mucida,Guann-Yi Yu,Sivakumar Vallabhapurapu,Jürgen Scheller,Stefan Rose-John,Hilde Cheroutre,Lars Eckmann,Michael Karin +11 more
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TLDR
It is demonstrated that IL-6 is a critical tumor promoter during early CAC tumorigenesis and the NF-kappaB-IL-6-Stat3 cascade is an important regulator of the proliferation and survival of tumor-initiating IECs.About:
This article is published in Cancer Cell.The article was published on 2009-02-03 and is currently open access. It has received 1913 citations till now. The article focuses on the topics: Proinflammatory cytokine & Intestinal mucosa.read more
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Immunity, Inflammation, and Cancer
TL;DR: The principal mechanisms that govern the effects of inflammation and immunity on tumor development are outlined and attractive new targets for cancer therapy and prevention are discussed.
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Macrophage Diversity Enhances Tumor Progression and Metastasis
Bin-Zhi Qian,Jeffrey W. Pollard +1 more
TL;DR: There is persuasive clinical and experimental evidence that macrophages promote cancer initiation and malignant progression, and specialized subpopulations of macrophage may represent important new therapeutic targets.
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STATs in cancer inflammation and immunity: a leading role for STAT3
TL;DR: Signal transducer and activator of transcription proteins are central in determining whether immune responses in the tumour microenvironment promote or inhibit cancer, and STAT3 is a promising target to redirect inflammation for cancer therapy.
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Coordinated regulation of myeloid cells by tumours
TL;DR: This work considers myeloid cells as an intricately connected, complex, single system and focuses on how tumours manipulate the myeloids system to evade the host immune response.
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The pro- and anti-inflammatory properties of the cytokine interleukin-6
TL;DR: It turns out that regenerative or anti-inflammatory activities of interleukin-6 are mediated by classic signaling whereas pro-inflammatory responses of interLEukin -6 are rather mediated by trans-signaling.
References
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Inflammation and cancer
Lisa M. Coussens,Zena Werb +1 more
TL;DR: It is now becoming clear that the tumour microenvironment, which is largely orchestrated by inflammatory cells, is an indispensable participant in the neoplastic process, fostering proliferation, survival and migration.
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Reciprocal developmental pathways for the generation of pathogenic effector TH17 and regulatory T cells.
Estelle Bettelli,Yijun Carrier,Wenda Gao,Thomas Korn,Terry B. Strom,Mohamed Oukka,Howard L. Weiner,Vijay K. Kuchroo +7 more
TL;DR: It is shown that IL-6, an acute phase protein induced during inflammation, completely inhibits the generation of Foxp3+ Treg cells induced by TGF-β, and the data demonstrate a dichotomy in thegeneration of pathogenic (TH17) T cells that induce autoimmunity and regulatory (Foxp3+) T Cells that inhibit autoimmune tissue injury.
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Recognition of Commensal Microflora by Toll-Like Receptors Is Required for Intestinal Homeostasis
Seth Rakoff-Nahoum,Justin C. Paglino,Fatima Eslami-Varzaneh,Stephen C. Edberg,Ruslan Medzhitov +4 more
TL;DR: It is shown that commensal bacteria are recognized by TLRs under normal steady-state conditions, and this interaction plays a crucial role in the maintenance of intestinal epithelial homeostasis and protection from injury.
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TGFβ in the context of an inflammatory cytokine milieu supports de novo differentiation of IL-17-Producing T cells
Marc Veldhoen,Richard J. Hocking,Christopher J. Atkins,Richard M. Locksley,Brigitta Stockinger +4 more
TL;DR: The data indicate that, in the presence of IL-6, TGFbeta1 subverts Th1 and Th2 differentiation for the generation ofIL-17-producing T cells.
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Stat3 as an Oncogene
Jacqueline Bromberg,Melissa H. Wrzeszczynska,Geeta Devgan,Yanxiang Zhao,Richard G. Pestell,Chris Albanese,James E. Darnell +6 more
TL;DR: Substitution of two cysteine residues within the C-terminal loop of the SH2 domain of Stat3 produces a molecule that dimerizes spontaneously, binds to DNA, and activates transcription.